Pellagra, a nutritional deficiency disorder of Niacin, characterized by classical 3 Dʼs (dermatitis, diarrhea, dementia) is rarely seen nowadays in its full glory. [1],[2],[3] We report a case of a 65-year-old female patient, receiving treatment for Glioblastoma multiforme referred to us with complaints of painful skin lesions present over sun exposed sites for the past one week. She was on temozolomide and phenytoin (100 mg/3 times a day).

The patient's examination revealed presence of well demarcated tender duskyerythematous, scaly plaques over dorsal aspect of hands, feet and face [Figure 1]a and b. The patient was also found to have atrophic glossitis. Rest of the patient's systemic examination including her neurological examination was within normal limits.

The patient was thoroughly investigated and found to have significant dimorphic anemia (Hb 7 gm). Rest of the patient's hematological and biochemical investigations were essentially within the normal limits and her antinuclear antibody (ANA) was reported negative. We could not get the patient's serum niacin estimation or estimation of urinary metabolites due to financial constraints. A histopathological examination from lesion showed hyperkeratosis, parakeratosis, and regular elongation of rete ridges, with dyskeratotic maturation and epidermal pallor and minimal mononuclear perivascular infiltrate [Figure 2].

Figure 2: Psoriasiform hyperplasia with dyskeratotic maturation and epidermal pallor. The staining is hematoxylin and eosin. Magnification is ×100

In view of the history, clinical and investigation findings, a diagnosis of phenytoin induced, pellagroid dermatitis was entertained. The patient was started on niacin supplementation, 150 mg thrice a day along with photo protection and other nutritional supplementation and was asked to continue rest of her medications. A marked improvement was seen in the patient's cutaneous lesions [Figure 3]a and b at four weeks follows up; she reported no further photosensitivity and continued to be asymptomatic for the past six months.

Niacin (Vitamin B3) is a precursors of coenzymes nicotinamide adenine dinucleotide (NAD) and NAD phosphate, which play a crucial role in essential oxidative and reductive metabolic reactions and DNA repair. [1],[4] The daily recommended allowance of niacin equivalent (NE) is 16 and 14 for men and women, respectively. [1],[4]

Niacin deficiency is known to manifest as pellagra, mostly reported from populations thriving on maize. Other conditions associated with niacin deficiency include chronic alcoholism, malabsorption, Hartnup disease and carcinoid syndrome. [2],[3],[4] Drugs implicated in manifesting niacin deficiency are antitubercular drugs (isoniazid, ethionamide, pyrazinamide), 5-fluorouracil, mercaptopurine and anticonvulsants (phenobarbital, carbamazepine, phenytoin). [3],[4],[5] The exact mechanism of pellagroid dermatitis precipitated by anticonvulsants is not known, although there have been postulates.

The diagnosis of pellagra is mostly based on a suggestive clinical setting. However, the classical triad may rarely be present in the same patient. Estimation of serum niacin levels or of urinary 2-pyridone/N 1 -methylnicotinamide levels (metabolite of niacin) are commonly used to confirm deficiency. [1],[2] Histopathological and electroencephalography examination can also be contributory. [1],[3]

As per World Health Organization (WHO) recommendation, nicotinamide 300 mg orally in divided doses or 100 mg parentally in divided doses should be given for 3-4 weeks. Neurological symptoms shows improvement within 24 to 48 h, but skin lesions may take 3 to 4 weeks to resolve, as was seen in our case. A maintenance dose with nicotinamide 50 to 100 mg/day is recommended. [5] This case is reported for its unique presentation and to highlight the importance of this under-reported, under-recognized and easily treatable complication of prolonged anticonvulsant usage.